Link and Phelan (1995) developed the theory of fundamental causes to explain why the association between
socioeconomic status (SES) and mortality has persisted despite radical changes in the diseases and risk
factors that are presumed to explain it. They proposed that the enduring association results because
SES embodies an array of resources, such as money, knowledge, prestige, power, and beneficial social
connections that protect health no matter what mechanisms are relevant at any given time. In this article,
we explicate the theory, review key findings, discuss refinements and limits to the theory, and discuss
implications for health policies that might reduce health inequalities. We advocate policies that encourage
medical and other health-promoting advances while at the same time breaking or weakening the link
between these advances and socioeconomic resources. This can be accomplished either by reducing
disparities in socioeconomic resources themselves or by developing interventions that, by their nature,
are more equally distributed across SES groups.

1.
Journal of Health and
Social Behavior
http://hsb.sagepub.com/
Social Conditions as Fundamental Causes of Health Inequalities : Theory, Evidence,
and Policy Implications
Jo C. Phelan, Bruce G. Link and Parisa Tehranifar
Journal of Health and Social Behavior 2010 51: S28
DOI: 10.1177/0022146510383498
The online version of this article can be found at:
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Phelan et al.
inequalities seen in earlier periods (i.e., deadly
infectious diseases such as diphtheria, measles,
typhoid fever, and tuberculosis fueled by overcrowding and poor sanitation in low socioeconomic status homes and communities) have been
virtually eradicated in the developed world. Rather
than disappearing, socioeconomic status (SES)
inequalities in mortality have persisted and now
reflect new major causes of death including cancers and cardiovascular illness, fueled by risk factors such as poor diet, inadequate exercise, and
smoking that are more common in lower SES
groups. Socioeconomic inequalities in health and
mortality have even survived concerted efforts to
eliminate them, such as institution of the United
Kingdom’s National Health Service, their vast
publicly-funded health care system (Black et al.
1982).
It is this persistence across time that Link and
Phelan (1995) aimed to explain with their theory of
fundamental causes. They reasoned that we cannot
claim to understand why health inequalities exist if
we cannot explain why they persist under conditions that should eliminate or reduce them, and if
we can understand why they persist, this may provide clues to the more general problem of the
causes of health inequalities. That is, the remarkable persistence of inequalities may provide a lever
for understanding the more general fact of their
existence.
In this article, we will explicate the theory as it
has developed over the past 15 years, review key
empirical findings, develop some refinements of
the theory, address potential limits of the theory,
and discuss implications for health policies that
might reduce health inequalities.
THE THEORY
The theory of fundamental causes is rooted in
Lieberson’s (1985) concept of basic causes, which
was first applied to the association between SES
and mortality by House and colleagues (House
et al. 1990, 1994). The theory has been developed
primarily by Link and Phelan (Link and Phelan
1995; Phelan et al. 2004; Link and Phelan, forthcoming), with significant elaboration and extension by Lutfey and Freese (2005).
The primary statement of the theory appeared
in 1995 in a previous special issue of the Journal
of Health and Social Behavior. According to Link
and Phelan (1995), a fundamental social cause of
health inequalities has four essential features. First,
it influences multiple disease outcomes, meaning
that it is not limited to only one or a few diseases
or health problems. Second, it affects these disease
outcomes through multiple risk factors. Third, it
involves access to resources that can be used to
avoid risks or to minimize the consequences of
disease once it occurs. Finally, the association
between a fundamental cause and health is reproduced over time via the replacement of intervening
mechanisms (Link and Phelan 1995). It is the persistent association of SES with overall health in the
face of dramatic changes in mechanisms linking
SES and health that led Link and Phelan to call
SES a “fundamental” cause of health inequalities.
The Central Role of Flexible Resources
for SES Inequalities in Health
According to the theory of fundamental causes, an
important reason that SES is related to multiple
disease outcomes through multiple pathways that
change over time is that individuals and groups
deploy resources to avoid risks and adopt protective strategies. Key resources such as knowledge,
money, power, prestige, and beneficial social connections can be used no matter what the risk and
protective factors are in a given circumstance.
Consequently, fundamental causes affect health
even when the profile of risk and protective factors
and diseases changes radically. If the problem is
cholera, for example, a person with greater
resources is better able to avoid areas where the
disease is rampant, and highly resourced communities are better able to prohibit entry of infected
persons. If the problem is heart disease, a person
with greater resources is better able to maintain a
heart-healthy lifestyle and get the best medical
treatment available. Because these resources can
be used in different ways in different situations, we
call them flexible resources.
It is their capacity to be used flexibly by individuals and groups that places resources of knowledge, money, power, prestige, and beneficial social
connections at the center of fundamental cause
theory. Their flexible use tells us why SES gradients tend to reproduce themselves over time. This
focus on resources and their deployment does not
deny the importance of antecedent causes of the
resources themselves that lie in the social, economic, and political structures of society. In fact,
fundamental cause theory is deeply connected to
the sociological study of stratification in this
way—the resources highlighted in fundamental
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cause theory must come from somewhere, and
theories of the origins of inequalities are the best
source for understanding these processes. To
understand how flexible resources might facilitate
the creation of new mechanisms linking SES and
health, consider the following example. Screening
for several cancers has become possible over the
past few decades, making it feasible to detect cancer or its precursors earlier, thereby helping to
prevent mortality from these cancers. Since the
screening procedures represent relatively recent
technological advances, one can imagine a time
before the procedures existed, when resources had
no bearing on access to cancer screening because
the procedures did not exist. There was no mechanism linking SES to screening access to health.
But after the screening procedures were developed, people with more resources could use those
resources to gain access to the life-saving screens.
Link et al. (1998) presented evidence from the
Behavioral Risk Factor Survey showing that
screening rates for cervical and breast cancer are
indeed associated with education and income.1 A
new mechanism had emerged to link social conditions to health outcomes. The idea is that this process extends beyond this example to many, many
others.
The flexible resources that are central to fundamental cause theory operate at both individual and
contextual levels. At the individual level, flexible
resources can be conceptualized as the “cause of
causes” or “risk of risks” that shape individual
health behaviors by influencing whether people
know about, have access to, can afford, and receive
social support for their efforts to engage in healthenhancing or health-protective behaviors. In addition, resources shape access to broad contexts that
vary dramatically in associated risk profiles and
protective factors. For example, a person with
many resources can afford to live in a high SES
neighborhood where neighbors are also of high
status and where, collectively, enormous clout is
exerted to ensure that crime, noise, violence, pollution, traffic, and vermin are minimized, and that
the best health-care facilities, parks, playgrounds,
and food stores are located nearby. Once a person
has used SES-related resources to locate in an
advantaged neighborhood, a host of healthenhancing circumstances comes along as a package deal. Similarly, a person who uses educational
credentials to procure a high-status occupation
inherits a package deal that is more likely to
include excellent health benefits and less likely to
involve dangerous conditions and toxic exposures.
In these circumstances, the person benefits in
numerous ways that do not depend on his or her
own initiative or ability to personally construct a
healthy situation; it is an “add on” benefit operative at the contextual level. These contexts may be
meso (families) or macro levels (a congressional
block that opposes changes in health care policy
that would shift the distribution of health care
away from high SES groups to the uninsured),
formal (employer or trade union) or informal
(social networks). The clearest example of fundamental cause theory occurs when groups explicitly
push for better health conditions for their members. But the health-enhancing use of group
resources can operate at a less explicit level. Consider Cockerham’s (2005) ideas about the influence of status groups on health lifestyles. According
to Cockerham, social norms and other social supports, such as the health-product industry, reinforce distinctive health lifestyles in different status
groups, and the lifestyles of high SES groups are
particularly healthy ones. In these instances status groups do not explicitly advocate for healthenhancing conditions, but rather members form
cultural practices around food, exercise, and
other health-related circumstances that influence
the behavior of status-group members. These
lifestyles are shaped by the extant stock of
health knowledge and pecuniary resources generally available in particular status groups—a
circumstance that generally leads to healthier
lifestyles in higher status groups. For example, it
is almost unheard of for snacks offered at meetings held at the Mailman School of Public
Health at Columbia University to not include
multiple varieties of fruits; Dunkin Donuts, in
contrast, are rare indeed. It is not as if the people
who order these snacks explicitly consider the
health impact of their choices each time a decision is made. Instead, cultural practices shaped
over time lead them to order the conventional,
and the conventional in this context is generally
healthy fare.
KEY EMPIRICAL FINDINGS
Empirical tests of the theory are not obvious or
straightforward. A demonstration of socioeconomic inequalities in health or mortality, even ones
that persists over time, does not in itself constitute
support for the theory. It is precisely the nearly
ubiquitous inverse association between SES and
mortality that the theory attempts to explain.
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Demonstrating this association in any particular
circumstances cannot adjudicate between fundamental causes and other possible explanations of
those facts.
Empirical support for the theory relies on evaluating the four essential features of a fundamental
cause of health inequalities (Link and Phelan
1995). In the following sections, we present key
findings bearing on each of these components:
(1) evidence that SES influences multiple disease
outcomes; (2) evidence that SES is related to multiple risk factors for disease and death; (3) evidence
that the deployment of resources plays a critical role
in the association between SES and health/mortality;
and (4) evidence that the association between SES
and health/mortality is reproduced over time via the
replacement of intervening mechanisms.
Evidence That SES Is Related to Multiple
Disease Outcomes via Multiple Risk Factors
The first two propositions are strongly supported
by empirical data. Low SES is related to a multiplicity of diseases and other causes of death. The
broad generality of this association can be summarized with two sets of facts: (1) Low SES is
related to mortality from each of the broad categories of chronic diseases, communicable diseases,
and injuries (Pamuk et al. 1998; National Center
for Health Statistics 2008), and (2) low SES is
related to mortality from each of the 14 major
causes of death in the International Classification
of Diseases (Illsley and Mullen 1985).
There is also clear evidence that SES is associated with numerous risk and protective factors for
disease and other causes of death, both currently
and in the past. These include smoking, sedentariness, and being overweight (Lantz et al. 1998;
Link 2008); stressful life conditions (Turner,
Wheaton, and Lloyd 1995; House and Williams
2000); social isolation (House and Williams 2000;
Ruberman et al. 1984); preventive health care
(Dutton 1978; Link et al. 1998); and crowded and
unsanitary living conditions, unsanitary water supplies, and malnutrition (Rosen 1979).
Lutfey and Freese (2005) describe this component of the theory as involving a “massive multiplicity of mechanisms.” They suggest that, because
fundamental cause processes are “holographic,”
such a multiplicity of mechanisms should be found
in all or most particular instances in which SES
and health outcomes are connected. Using an
ethnographic analysis, they use the example of
routine diabetes care in two socioeconomically
contrasting clinics to articulate several concrete
ways in which differential health outcomes emerge
in the two clinics. For example, the clinic serving
higher SES patients provided better continuity of
care, and the higher SES patients encountered
fewer costs of complying with treatment regimens
and had more knowledge about diabetes. Similar
analyses conducted in a variety of contexts relating
to treatment or prevention of a variety of diseases
would enrich our understanding of the pathways
through which SES influences health and longevity.
Evidence that the Deployment of Resources
Plays a Critical Role in the Association
between SES and Health
Central to fundamental cause theory is the idea that
resources of money, knowledge, power, prestige,
and beneficial social connections are critical to
maintaining a health advantage. Empirically testing the importance of resources per se is difficult,
because it requires the identification of situations
in which the ability to use socioeconomic resources
can be analytically separated from SES itself (e.g.,
situations in which high SES persons are prevented
from using their resources to gain a health advantage). If the utilization of resources is critical in
maintaining health or prolonging life, then in situations in which the resources associated with
higher status are of no use, high SES should confer
no advantage, and the usually robust association
between SES and health or mortality should be
greatly reduced.
One such situation occurs when the causes and
cures of fatal diseases are unknown. In these circumstances, socioeconomic resources cannot be
used to avoid death due to these diseases, because
it is not known how the resources should be
deployed. Thus, to the extent that the ability to use
socioeconomic resources is critical in maintaining
SES inequalities in mortality, there should be
strong SES gradients in mortality for causes of
death that are highly preventable —for which we
have good knowledge and effective measures for
prevention or treatment. However, for causes of
death about which we know little regarding prevention or treatment, SES gradients in mortality
should be much weaker. Consistent with this prediction, Phelan et al. (2004) found that socioeconomic inequalities in mortality were significantly
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more pronounced for causes of death that were
reliably rated by two physician-epidemiologists as
being highly preventable (such as lung cancer and
ischemic heart disease), and thus more amenable
to the application of flexible resources than for
causes that were rated as not very preventable (such
as brain cancer and arrhythmias). Although they do
not address or explicitly test fundamental cause
theory, three other studies that reported evidence
on this issue also found that the SES-mortality
association was stronger for preventable causes of
death (Dahl, Hofoss, and Elstad 2007; Marshall
et al. 1993; Song and Byeon 2000).
Evidence for the validity and generality of
these findings is strengthened by another study that
employed a similar research strategy but (1) examined a different set of causes of death, (2) confined
attention to treatment rather than including prevention, (3) used a different and more objective measure of amenability to treatment, and (4) examined
racial and ethnic differences as opposed to socioeconomic ones.2 Tehranifar et al. (2009) identified,
prior to hypothesis testing, cancers that are more or
less amenable to treatment and examined whether
racial-ethnic differences in disease-specific mortality varied according to the degree to which that
disease is amenable to available medical intervention. This study used five-year survival rates for 53
different cancer sites as a measure of effectiveness
of treatment and/or early detection methods. Consistent with fundamental cause theory, survival
disparities comparing disadvantaged minority
groups (African Americans, American Indians, and
Hispanics) to whites were substantially greater for
cancers that were more amenable to treatment
(e.g., cancers with five-year relative survival rates
≥ 70%, such as bladder, breast, and prostate cancers) than they were for cancers that were less so
(e.g., cancers with five-year relative survival rates
< 40%, such as liver, pancreatic, and esophageal
cancers).
These studies show that, somewhat ironically,
one way in which fundamental cause theory can be
tested is by looking for exceptions to the strong
SES gradient in health or mortality that is almost
always observed—exceptions in which the ability
to use resources to gain a health advantage is
blocked. In these examples, the use of socioeconomic resources to improve health is blocked
because risk factors are unknown and treatments
do not exist (Phelan et al. 2004; Tehranifar et al.
2009). Other situations in which resources may be
unhelpful or even harmful may be exploitable for
testing of the theory. Examples are situations in
which prevailing medical recommendations are
subsequently discovered to be harmful (Carpiano
and Kelly 2007) and the case of old age, when the
growing frailty of the body may place limits on the
effectiveness of interventions (Phelan et al. 2004).
Evidence That the Association between SES
and Health/Mortality Is Reproduced over
Time via the Replacement of Intervening
Mechanisms
The fourth essential feature of SES as a fundamental
cause of health inequalities is that the association
between SES and health/mortality is reproduced
over time via the replacement of intervening mechanisms. This key element of the theory arose from
two sets of observations: (1) The SES-mortality
association persisted over time despite the decline
of mechanisms (e.g., poor sanitation and widespread death from infectious disease) that formerly
provided important links between SES and mortality; and (2) new, previously weak or absent
mechanisms currently link SES and mortality (e.g.,
smoking, exercise, diet, and cardiovascular disease). These observations are consistent with the
idea that socioeconomic inequalities in health are
reproduced via the replacement of intervening
mechanisms. To more fully evaluate this component of the theory, however, more direct evidence
was needed showing the emergence of new mechanisms. In particular, the theory predicts that new
mechanisms arise following the development of
new knowledge or medical intervention related to
some disease, because higher SES individuals and
groups are better equipped to take advantage of the
new knowledge. Therefore, a key empirical question is whether the SES-health gradient shifts in
favor of high SES individuals following the development of new knowledge. This evidence is particularly persuasive if the health outcome for
which a shifted gradient is observed is directly
related to the emergent knowledge, for example, if
an advance in heart disease treatment furthers the
advantage of high SES individuals in terms of
heart disease mortality. Just as important is evidence that, in the absence of advances in knowledge, the SES gradient in relevant health outcomes
remains fairly steady.
Several such analyses have now been conducted. Phelan and Link (2005) examined selected
causes of death for which great strides in prevention or treatment were made over the last half of
the twentieth century (heart disease, lung cancer,
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and colon cancer), and for which much less
progress had been made over the same period
(brain cancer, ovarian cancer, and pancreatic cancer). Looking at age-adjusted death rates by race
and by county-level SES, they reported that, for
the causes of death where little had been learned
about treatment or prevention, mortality rates
stayed fairly steady, and the degree of inequality
based on race and SES stayed fairly steady as well.
By contrast, for the causes of death where gains in
treatment and prevention had been significant,
overall mortality rates declined while race and SES
gradients shifted in the direction of relatively
higher mortality for the less advantaged group.
Subsequent studies have gone much further in
drawing specific connections between gains in
knowledge and subsequent changes in relevant
disease outcomes. Carpiano and Kelly (2007) analyzed changes in breast cancer incidence following
the widely publicized findings from the Women’s
Health Initiative (WHI) that linked hormone
replacement therapy to increased breast cancer risk
(Haas et al. 2004). In the following two years,
consistent with the racial pattern in the use of hormone replacement therapy (Haas 2004; Hulley
et al. 1998), breast cancer incidence among white
women age 50 and older, the age group most likely
to have been using hormone therapy before the WHI
study results were publicized, dropped precipitously, while incidence among black women in that
age group stayed fairly steady (Carpiano and Kelly
2007). These findings were confirmed by another
study that also considered county-level median
household income and breast tumor estrogen (ER)
receptor status (Krieger, Chen and Waterman 2010).
That study found the decline in breast cancer incidence after the WHI study publication to be limited to white women, aged 50 and older, who were
residents of high income counties and had estrogen-positive breast tumors (the type of tumor most
likely to be affected by hormone replacement).
Chang and Lauderdale (2009) studied the
impact of statins (an effective and expensive medication to lower cholesterol) on socioeconomic
gradients in cholesterol levels. Using nationally
representative data from 1976 to 2004, they found
that those with higher income initially had higher
cholesterol levels, but that the SES-cholesterol
association then reversed and became negative in
the era of widespread statin use.
Link (2008) traced changes in knowledge,
beliefs, and behavior that followed the discovery
of a causal link between cigarette smoking and
lung cancer, and that eventually led to strong
socioeconomic gradients in smoking. Scientific
evidence strongly linking smoking to lung cancer
emerged in the early 1950s. To assess changes that
may have occurred in the decades following the
production of this new knowledge, Link (2008)
analyzed multiple public opinion polls assessing
smoking beliefs and behaviors. Evidence from the
first surveys conducted just as the scientific evidence was emerging in 1954 showed that, while
most people had heard about the findings, only a
minority believed that smoking was a cause of
lung cancer, and no educational gradient in this
belief was evident. Nor was smoking behavior
strongly linked to educational attainment in 1954.
Over the subsequent 45 years, as people began to
adopt the belief that smoking is a cause of lung
cancer, sharp educational gradients opened up in
this belief. Additionally, people of higher education were less likely to start smoking and more
likely to quit, thereby generating a strong SES
gradient in smoking behavior (Link 2008). A new
and powerful mechanism linking SES to an important health behavior had emerged.
The studies just described are particularly valuable for their ability to pinpoint temporal connections between particular developments in
knowledge and technology surrounding specific
diseases, on the one hand, and changes in SESrelated health gradients predicted by the theory, on
the other. Moreover, these studies address major
diseases that are important causes of death. However, there is always the possibility that these cases
are not representative of the situation that holds
more generally when new health knowledge or
technology develops. For this reason, the more
systematic and comprehensive analysis of Glied
and Lleras-Muney (2008) is particularly valuable.
This study provides evidence that the results of the
case studies reported above are indeed generalizable. Like Phelan et al. (2004) and Tehranifar et al.
(2009), Glied and Lleras-Muney conducted a systematic test based on a comprehensive set of diseases. In fact, Glied and Lleras-Muney repeated
their analysis with two separate data sets: the Mortality Detail Files from the National Center for
Health Statistics, and the Surveillance Epidemiology
and End Results cancer registry. They operationalized the development of life-saving knowledge and
technology, or “innovation,” in two ways. In the
first they used the rate of change in mortality over
time to indicate progress in addressing mortality
due to particular diseases, the assumption being
that the greater the decline in mortality, the greater
the progress that has been made. In the second,
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they used the number of active drugs approved
to treat particular diseases, with the assumption
that more progress has been made where more
new drugs have been developed to treat disease.
They found, consistent with the theory of fundamental causes, that educational gradients became
larger for diseases where greater innovation had
occurred.
In summary, evidence has accumulated that is
consistent with each of the four components of
fundamental cause theory. Empirical testing of the
theory is accelerating, and studies are now being
conducted by researchers other than the theory’s
originators. This is a desirable development, as it
raises confidence that the theory is being subjected
to scientific scrutiny.
RETURNING TO THE THEORY:
REFINEMENTS AND LIMITATIONS
Refinements to Fundamental Cause Theory
The theory has two sets of implications for continuity and change in health inequalities over time.
The theory’s basic principle—that a superior collection of flexible resources held by higher SES
individuals and the collectivities to which they
belong allow those of higher SES to avoid disease
and death in widely divergent circumstances—
leads to the prediction that, at any given time,
greater resources will produce better health, and
consequently inequalities in health and mortality
will persist as long as resource inequalities do.
At the same time, this long-term stability in the
association between SES and health/mortality
results from the amalgamation of effects across
many specific processes and conditions. New
knowledge and technology relating to innumerable
diseases emerges constantly. The nature of the new
knowledge varies, and the social conditions in
which this knowledge emerges also vary. As a
result, while in general new knowledge and medical development about a disease will lead to a shift
in the disease gradient in favor of higher SES individuals and groups, they will not all have an identical impact on this gradient. Another reason for the
long-term stability in the SES-mortality association is that old mechanisms wane to be replaced by
new ones. Again, the demise of mechanisms is not a
uniform process: Some mechanisms have long
lives, others short ones. In this section, we take steps
toward understanding some of the conditions that
lead to variations in the processes of mechanism
generation and demise. Our aim is not only to
strengthen the theory but to understand how it may
be possible to weaken new mechanisms connecting SES and disease/mortality, and how old ones
may be undermined.
Specifying Conditions that Modify the
Impact of New Knowledge on Health
Inequalities
The situation that most clearly exemplifies fundamental cause processes is one in which we initially
know nothing about how to prevent or cure a disease, and there is no association between SES and
morbidity or mortality due to that disease. Then,
upon discovery of modifiable risk or protective
factors, an inverse association between SES and
the disease in question emerges. But other situations that differ from this prototype are not only
possible but to be expected.
One factor that should modify the impact of
emergent knowledge is the pre-existing SES distribution of the disease at the time of a new advance
in prevention or treatment.3 The pre-existing association between the disease and SES is unlikely to
be null for two reasons. First, when new knowledge and technology emerge, it is often the case
that prior knowledge and technology have already
shaped the association between SES and disease;
the new knowledge will further shape this association. Second, even in the absence of previous
knowledge about its risk and protective factors, a
disease may be influenced by factors that are associated with SES, either directly or inversely. For
example, before cholesterol was identified as a risk
factor for cardiovascular disease its levels were
likely higher in higher SES populations because
such populations had greater access to relatively
expensive fatty foods.
The reason that prior associations between risk
factors or diseases and SES are important for fundamental cause theory is that the new knowledge
has greater utility for those who have the disease or
risk factor. Notably, if the initial association
between SES and the disease is inverse such that
people of lower SES are at greater risk, an effective intervention can reduce inequalities in that
disease. This is because more people of low SES
are likely to benefit from the intervention, because
more of them have the disease initially. This can be
true even if persons of higher SES who have the
disease are more likely to gain access to and benefit from the intervention than lower SES persons
who have the disease. We call this a “give back
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effect” (Link and Phelan, forthcoming), because
the initial inverse SES-to-disease association provides a starting point that allows the new knowledge about the disease to “give back” some
equality even though it may also exemplify a fundamental cause process in which the knowledge is
not distributed equally across socioeconomic
groups. For example, smoking is a risk factor that
has been influenced by knowledge of its harmful
effects such that what was once a direct SES-tosmoking association has become a sharply graded
inverse association, and one reason that SES is
related to smoking-related diseases.
In this context a “give back” effect would arise
if a new intervention blocked the effect of smoking
on heart disease or lung cancer mortality. Even if
this new intervention was itself maldistributed by
SES, a “give back” effect might arise because
smoking is so much more common in low SES
populations; in other words, there are more people
at the low end who can benefit from the new intervention. Importantly, from a fundamental cause
perspective, if the intervention had been discovered earlier, before an SES-to-disease association
in smoking emerged, and if the intervention had
been maldistributed by SES at that time, the intervention would have created an inverse association
between SES and lung cancer or heart disease.
Mechanism Demise and Death
Whereas it is understandable that empirical tests
have focused on the creation of mechanisms that
produce health inequalities, fundamental cause theory is predicated on the idea that mechanisms are
replaced. Replacement requires that old mechanisms wane in importance over time. In fact, the
theory emerged in part because prominent riskfactor mechanisms associated with vicious infectious
diseases declined in significance as germ theory,
improved sanitation, and vaccination came into
existence. Thus, understanding the demise and death
of mechanisms linking flexible resources to disease
is an important area that needs more development
and testing. We offer two examples that may help
others develop this area of inquiry more fully.
Salk’s discovery of the polio vaccine is an
example of a mechanism that was very short-lived.
Before his discovery, people of all resource levels
could be afflicted, including, for example, President Franklin Roosevelt. After the discovery,
resource-rich individuals were more likely to
receive the vaccine and be protected. A mechanism
linking resources to health existed, but only for a
short time. The vaccine was quickly approved for
widespread distribution to the U.S. population, and
polio was virtually eradicated here. Other mechanisms remain potent for a very long time. For,
example the discovery of the pap test for the early
detection and prevention of cervical cancer has
existed since the 1940s. Early on, access to the test
was shaped by flexible resources creating an inequality in the use of this life-saving screen that
remains prominent today. As these examples suggest, some mechanisms become long-lasting while
others have short lives. If we can understand what
leads to the demise of mechanisms, and especially
how that decline is related to flexible resources, we
may open avenues to speed such a demise and
reduce health inequalities. Indeed, much of the
public health significance of fundamental cause
theory may reside in understanding how the link
between flexible resources and health-relevant risk
and protective factors has been broken.
Limits on Fundamental Cause Theory:
Countervailing Mechanisms
Whereas the previous sections elaborated fundamental cause theory, here we consider conditions
that place limits on the theory.
We believe readers will agree that health and
longevity are desirable, but they are not all that a
person may want. Other things being equal, those
with more resources can be expected to deploy
those resources to increase health. But there are
undoubtedly situations in which the goals of health
and long life compete with and may cede dominance to other important life goals. Perhaps desiderata such as power, manliness, or beauty are
sometimes more powerful motivators than health,
and are pursued to the detriment of health. Lutfey
and Freese (2005) refer to these competing goals
as “countervailing mechanisms.” The potential for
countervailing mechanisms does not threaten the
truth-value of fundamental cause theory, because
“fundamental relationships do not require that all
of the pathways between X and Y support the relationship. The only requirement is that the effects of
[countervailing] mechanisms are cumulatively
smaller than the effects of mechanisms producing
the fundamental relationship” (Lutfey and Freese
2005:1365). However, to the extent that countervailing mechanisms are called upon post hoc to
explain results that do not support the theory,
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countervailing mechanisms pose a challenge to the
falsifiability of the theory. For this reason, as well
as for the fuller understanding of health inequalities, it is desirable to attend to countervailing
mechanisms systematically, as Lutfey and Freese
argue, and attempt to move the consideration of
countervailing mechanisms from post hoc to a
priori.
We first note that the connection between SES
and health is an extremely powerful one and that
goals that successfully compete with those of
health and long life must surely be quite potent.
For example, the goal of health attainment has
been powerful enough to override or socially
reconstruct many aspects of pleasure and pain—
which would seem to be basic and powerful forces
in their own right—among the socioeconomically
privileged. Erstwhile pleasures such as well marbled steaks are eschewed by higher SES groups in
favor of sushi-grade tuna. Similarly, in the past,
exhausting physical activity was considered something that high SES people were fortunate enough
to be able to avoid. Now, “no pain no gain” prevails in the most expensive health clubs. Cigarette
smoking, although highly addictive, as well as
sexual practices that increase the risk of HIV/
AIDS, have also been significantly altered by high
SES groups in the name of health attainment. We
also note that the goals of health and longevity are
strongly supported by social norms and other
forms of social support among high status groups
as part of the beneficial health lifestyle associated
with high SES (Cockerham 2005). We suggest that
the power of health attainment to shape the behavior of high SES individuals is largely due to these
social forces, and we propose that successful countervailing mechanisms are also likely to be embedded in strong social norms and support.
One such motivation that may meet these conditions is status attainment. In Lutfey and Freese’s
(2005) ethnographic analysis of diabetes treatment, the pursuit of status, for example, occupational success or staying thin, sometimes led higher
SES diabetic patients to behave in ways detrimental to the management of their disease. Similarly,
Courtenay (2000) suggests that signifiers of masculinity such as the denial of weakness and engagement in risky or aggressive behavior often
undermine men’s health. Thus, the pursuit of masculine status may help explain the fact that women,
who are generally lower resourced than men, live
longer than men, a fact that would not be predicted
by fundamental cause theory.4 It seems, then, that
status pursuit is one potential countervailing mechanism to the SES-health association. In the context
of particular empirical studies, researchers may be
able to consider a priori whether the situation
under study is one in which the goals of health and
social status are likely to collide. Additional
motivations that might potentially be powerful
enough to operate as countervailing mechanisms to
SES include power, affiliation, self-esteem, identity, freedom, creation, and leisure (Maslow 1943;
Max-Neef, Elizalde, and Hopenhayn 1989).
Note that, in most circumstances, we would
expect the goal of good health to be compatible
with goals of power, self-esteem and so on, and we
would expect higher SES individuals to use their
resources to achieve more of all these desiderata
than lower SES persons would be able to. Still, the
example of status pursuit as a countervailing
mechanism suggests that there will be instances
when other powerful motivations that are more
readily attained by high SES persons work to the
detriment of health. In those situations, the usual
association between resources and health should
be attenuated. Also note that these countervailing
mechanisms may create conditions when SES will
not operate as a fundamental cause of health and
mortality, but they do not negate the power of SES
as a fundamental cause of unequal life chances
more generally.
IMPLICATIONS FOR HEALTH
POLICY
The fundamental cause approach leads to very
different policies for addressing health inequalities than does an individually oriented risk-factor
approach. The latter asks us to locate modifiable
risk factors that lie between distal cause (such as
SES) and disease, and to intervene in those risk
factors. By addressing intervening factors, the
logic goes, we will eliminate health disparities.
Our approach points to the pitfalls of this logic
and suggests that developing new interventions,
even when beneficial to health, is very likely to
increase social inequalities in health outcomes. The
idea that medical progress often leads to increased
health inequality leads to an obvious conundrum:
Must we choose between improving overall levels
of health and reducing inequalities in health? Some
argue that continued inequalities in health outcomes are acceptable as long as overall health
improves or that some improvement is achieved for
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most social groups. We, on the other hand, are committed to reducing health inequalities, but it seems
wrong-headed to oppose advances in health knowledge and technology because those may increase
inequalities. We see no reason not to make both
outcomes important goals, simultaneously pursuing better overall health and reduced inequalities.
We suggest some general strategies that we
believe will lead to improved overall population
health without further widening social inequalities
in health. Our approach points to policies that
encourage advances while breaking or weakening
the link between these advances and socioeconomic resources, either by reducing disparities in
socioeconomic resources themselves, or by developing interventions that, by their nature, are more
equally distributed across SES groups.
Reduce Resource Inequalities
The first recommendation falls outside the explicit
domain of health policy, but according to fundamental cause theory is intimately tied to it. The
theory stipulates that people and collectivities use
their knowledge, money, power, prestige, and
social connections to gain a health advantage, and
thereby reproduce the SES gradient in health. The
most direct policy implication of the theory is that,
if we redistribute resources in the population so as
to reduce the degree of resource inequality,
inequalities in health should also decrease. Policies
relevant to fundamental causes of disease form a
major part of the national agenda, whether this
involves the minimum wage, housing for homeless
and low-income people, capital-gains and estate
taxes, parenting leave, social security, head-start
programs and college-admission policies, regulation of lending practices, or other initiatives of this
type. We argue that all these policies are healthrelevant policies and that understanding how they
are relevant should be claimed as an essential part
of the domain of medical sociology.
Contextualize Risk Factors
Potential interventions that seek to change individual risk profiles should first identify factors that put
people at risk of risks, for example, power disadvantages that prevent some people from adopting safe
sex strategies or neighborhood environments that
make healthful foods unavailable. This will avoid
the enactment of interventions aimed at changing
behaviors that are powerfully influenced by factors
left untouched by the intervention.
Prioritize the Development of Interventions
that Do Not Entail the Use of Resources or
that Minimize the Relevance of Resources
As we seek to create interventions to improve
health, we need to ask if an intervention is something that anyone can potentially adopt, or whether
the benefit will only be available to people with the
necessary resources. Fundamental cause theory
suggests that health inequalities based on SES can
be reduced by instituting health interventions that
automatically benefit individuals irrespective of
their own resources or behaviors. Examples are the
manufacture of automobiles with air bags as
opposed to relying on the use of seatbelts; providing health screenings in schools, workplaces, and
other community settings rather than only through
private physicians; providing health care to all
citizens rather than only to those with the requisite
resources; requiring window guards in all high-rise
apartments rather than advising parents to watch
their children carefully; thoroughly inspecting
meat rather than advising consumers to wash cutting boards and cook meat thoroughly; adding folic
acid to grains rather than recommending that supplements be taken by pregnant women to prevent
neural tube defects in developing embryos; requiring landlords to keep homes free of lead paint
hazards rather than warning parents to protect their
toddlers from chipped paint. In some cases, such as
this last example, existing risks will be greater in
low-income neighborhoods and contexts, and special enforcement of these policies may be required
in those contexts. In each example, the former
solution does not give an advantage to those with
greater resources, because individual resources are
unrelated and irrelevant to benefiting from the
intervention.
However, even if we become far more creative
in developing contextually based interventions
that blanket an entire population with health benefit, addressing many health problems will still
require individual resources and action. In these
cases, resource-rich persons are likely to fare better. Even in these cases, however, we can influence
the trajectory of inequalities by attending to the
type of interventions we adopt. When we create
interventions that are expensive, complicated and
time-consuming to carry out, and difficult to distribute broadly, we are likely to create health
disparities (Chang and Lauderdale 2009). Conversely, to the extent that we develop interventions
that are relatively affordable and easy to disseminate and use, we should be able to reduce the
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degree to which new interventions give advantage
to high SES persons. Goldman and Lakdawalla
(2005) analyzed two case studies supporting the
idea that the introduction of difficult-to-implement
treatments (in their analysis, HAART treatment for
HIV/AIDS) lead to increased SES inequalities in
health outcomes, whereas treatments that are simpler and require less effort (in their analysis, betablockers to reduce hypertension) reduce such
inequalities. As Chang and Lauderdale (2009) suggest, this principle should also apply to cost: New
interventions that are less expensive should result
in smaller SES-based health inequalities than
those that are more expensive. Chang and Lauderdale also point out, importantly, that, “technologies that have the potential to contract disparities
will not do so unless they also diffuse broadly”
(Chang and Lauderdale 2009:257). We add that a
necessary ingredient of successful diffusion will
be broadly disseminated and clearly stated information about how an intervention can help one’s
health, where that intervention is available,
whether and how much of it is covered by health
insurance plans, and, if not, how much it will cost
individuals.
CONCLUSION
The theory of fundamental causes attempts to
explain why the association of SES to health and
mortality has persisted despite the demise of risk
factors and diseases that appeared to explain the
association. Mounting evidence in support of the
theory of fundamental causes begins to suggest
that the theory is not just an interesting idea but
very possibly a valid explanation of persistent SES
inequalities in health and mortality. We believe
this empirical support warrants the investment of
medical sociologists in (1) further empirical analyses using a variety of methodologies to give
greater weight to the body of research, to specify
and elaborate the processes at work, and to find
conditions that may block these processes and
(2) developing elaborations, extensions, and modifications of the theory itself. We also believe the
accumulated evidence warrants serious attention
to the implications of the theory for health policy.
Those implications are that, to achieve greater
equality in matters of life, death, and health, the
connection between socioeconomic resources and
health-beneficial preventive measures and treatments must be broken or diminished, by reducing
the magnitude of inequalities in socioeconomic
resources themselves and/or by minimizing the
extent to which socioeconomic resources buy a
health advantage. By attending to these principles,
we believe we can move toward the important
dual goals of continuing to improve overall population health while distributing that health more
equally.
FUNDING
This work was supported by a Young Investigator Award
granted to Professor Tehranifar by the Lance Armstrong
Foundation.
NOTES
1. We acknowledge recent debate and changes in guidelines with regard to screening interval and age at
initiation of screening mammography and pap tests.
However, convincing evidence supports the effectiveness of these screens in reducing cancer mortality and
morbidity (U.S. Preventive Services Task Force
2009; ACOG Committee on Practice Bulletins—
Gynecology 2009).
2. Fundamental cause theory was developed to explain
the enduring effects of SES on health and mortality. It
is possible that other social statuses, such as race, ethnicity, or gender, also have enduring associations with
resources of money, knowledge, power, prestige, and
beneficial social connections, and with health and
mortality, and that they may also operate as fundamental causes. Even if not, however, race and
ethnicity are currently strongly related to resources
and consequently would be expected to behave similarly to SES in analyses such as Tehranifar’s
(Tehranifar et al. 2009), which focus on the current
health context.
3. We thank David Mechanic for this insight.
4. Recent research suggests that, when health behaviors
of women come to resemble those of men more
closely, the female mortality advantage declines
(Preston and Wang 2006).
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Bios
Jo C. Phelan is professor of sociomedical sciences at the
Mailman School of Public Health of Columbia University.
Her research interests include social stigma, conceptions
of mental illness, the impact of the “genetics revolution”
on the stigma of mental illness, attitudes and beliefs relating to social inequality and its legitimation, and social
inequalities in health and mortality. In collaboration with
Bruce Link, she developed the argument that frames social
conditions as fundamental causes of disease.
Bruce G. Link is professor of epidemiology and sociomedical sciences at the Mailman School of Public Health
of Columbia University, and a Research Scientist at New
York State Psychiatric Institute. His interests include the
nature and consequences of stigma for people with mental
illnesses, the connection between mental illnesses and
violent behaviors, and explanations for associations
between social conditions and morbidity and mortality.
Parisa Tehranifar is assistant professor of epidemiology
at the Mailman School of Public Health of Columbia University. Her research combines social science and
epidemiologic perspectives and methods to studies of
social inequalities in cancer and other chronic disease
risk.
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